title: Myocardial stretch induced by increased left ventricular diastolic pressure preconditions isolated perfused hearts of normotensive and spontaneously hypertensive rats.
abstract: OBJECTIVE
  The aim of our study was to determine whether myocardial stretch (non-ischemic stress) could precondition isolated perfused hearts of both normotensive Wister-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR).
  
  
  METHODS
  The perfused hearts in Langendorff mode were subjected to 30 min of global no-flow ischemia followed by 30 min of reperfusion. Left ventricular developed pressure (LVDP) and end-diastolic pressure (LVEDP) were measured. In the control group, LVEDP was set at 10 mmHg. In the stretch group, LVEDP was increased to 30 or 60 mmHg for 5 min before 30 min of ischemia. In the ischemic preconditioning group, the hearts were exposed to two cycles of a 5-min period of ischemia before 30 min of ischemia. Myocardial lactate contents were measured at the baseline and at the end of the 60 mmHg stretch.
  
  
  RESULTS
  Hemodynamic parameters of LVDP and LVEDP at 30 min of reperfusion improved in the stretch group (LVEDP of 60 mmHg) and the ischemic preconditioning group. Coronary flow did not decrease during the stretch. Recovery of the coronary flow during reperfusion was better in the stretch and ischemic preconditioning groups. Postischemic contractile function was better in WKY rats than in SHR. Myocardial lactate contents at the end of 60 mmHg stretch were negligible.
  
  
  CONCLUSIONS
  Myocardial stretch induced by increasing LVEDP preconditioned isolated perfused hearts of both WKY rats and SHR, via mechanisms not involving myocardial ischemia during stretch.
authors.affiliation: Second Department of Medicine, Kyoto Prefectural University of Medicine, Japan.
authors.forename: C
authors.initials: C
authors.lastname: Nakagawa
authors.forename: J
authors.initials: J
authors.lastname: Asayama
authors.forename: M
authors.initials: M
authors.lastname: Katamura
authors.forename: S
authors.initials: S
authors.lastname: Matoba
authors.forename: N
authors.initials: N
authors.lastname: Keira
authors.forename: A
authors.initials: A
authors.lastname: Kawahara
authors.forename: K
authors.initials: K
authors.lastname: Tsuruyama
authors.forename: T
authors.initials: T
authors.lastname: Tanaka
authors.forename: M
authors.initials: M
authors.lastname: Kobara
authors.forename: K
authors.initials: K
authors.lastname: Akashi
authors.forename: B
authors.initials: B
authors.lastname: Ohta
authors.forename: T
authors.initials: T
authors.lastname: Tatsumi
authors.forename: M
authors.initials: M
authors.lastname: Nakagawa
mesh_terms: D000818:Animals; D001794:Blood Pressure; D003402:Creatine Kinase / Q000032:analysis; D006973:Hypertension / Q000201:enzymology / Q000378:metabolism / Q000503:physiopathology*; D066298:In Vitro Techniques; D019157:Ischemic Preconditioning, Myocardial; D007773:Lactates / Q000032:analysis; D008297:Male; D017202:Myocardial Ischemia / Q000201:enzymology / Q000378:metabolism / Q000503:physiopathology; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism; D010477:Perfusion; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D016277:Ventricular Function, Left
chemical_list: D007773:Lactates; D003402:Creatine Kinase